Cardiac function is a measure of the overall effectiveness of the cardiac system of a patient and is typically represented in terms of, one or more of, stroke volume, cardiac output, end-diastolic volume, end-systolic volume, ejection fraction or cardiac output index. Stroke volume is the amount of blood ejected from the left ventricle during systole. Cardiac output is the volume of blood pumped by the left ventricle per minute (or stroke volume times the heart rate). End-diastolic volume is the volume of blood in the chamber at the end of the diastolic phase, when the chamber is at its fullest. End-systolic volume is the volume of blood in the chamber at the end of the systolic phase, when the chamber contains the least volume. Ejection fraction is percentage of the end-diastolic volume ejected by the ventricle per beat. Cardiac index is the volume of blood ejected per minute normalized to the body surface area of the patient. Other factors representative of cardiac function include the contractility of the left ventricle or the maximum rate of change of pressure with time (i.e. max dP/dt).
Overall cardiac function should be carefully monitored in patients with pacemakers or ICDs, particularly patients suffering from heart failure. Heart failure is one of the most widespread and devastating cardiac afflictions, currently affecting approximately 15 million people worldwide, including over 5 million in the United States. In the U.S., approximately 450,000 new patients are diagnosed with heart failure each year and the majority die within five years of diagnosis. One factor that contributes to heart failure is asynchronous activation of the ventricles such that the mechanical contraction is not coordinated effectively thus compromising cardiac function. As a result, the pumping ability of the heart is diminished and the patient experiences shortness of breath, fatigue, swelling, and other debilitating symptoms. The weakened heart is also susceptible to potentially lethal ventricular tachyarrhythmias. A decrease in cardiac function can result in a progression of heart failure. In many cases, pacing control parameters of the pacemaker or ICD can be adjusted to help improve cardiac function and reduce the degree of heart failure effectively reducing symptoms and improving the quality of life.
In view of the importance of maintaining adequate cardiac function, it would be desirable to provide improved techniques for use with pacemakers or ICDs for monitoring cardiac function and for automatically adjusting pacing parameters to optimize cardiac function and reduce the degree of heart failure. It is to this end that aspects of the invention are generally directed.
One particularly promising technique for reducing the risk of heart failure is “ventricular resynchronization therapy”, which seeks to normalize asynchronous cardiac electrical activation and the resultant asynchronous contractions by delivering synchronized pacing stimulus to both ventricles using pacemakers or ICDs equipped with biventricular pacing capability. The stimulus is synchronized so as to help to improve overall cardiac function. This may have the additional beneficial effect of reducing the susceptibility to life-threatening tachyarrhythmias. With conventional resynchronization therapy, an external Doppler-echocardiography system may be used to noninvasively assess cardiac function. It can also be used to assess the effectiveness of any programming changes on overall cardiac function.
Then, biventricular pacing control parameters of the pacemaker or ICD are adjusted by a physician using an external programmer in an attempt to synchronize the ventricles and to optimize patient cardiac function. For example, the physician may adjust the interventricular delay, which specifies the time delay between pacing pulses delivered to the right and left ventricles, in an attempt to maximize stroke volume. To assess the effectiveness of any programming change, Doppler-echocardiography, impedance cardiography or some other independent measure of cardiac function is utilized.
However, this evaluation and programming requires an office visit and is therefore a timely and expensive process. It also restricts the evaluation to a resting state, commonly with the patient in a supine position. As such, the system is not necessarily optimized for activity, for the upright position, for other times of day since there may also be a circadian rhythm to cardiac function. It is known that heart rate and blood pressure have a diurnal variation. In a study by Chew and colleagues (See: “Overnight Heart Rate And Cardiac Function In Patients With Dual Chamber Pacemakers”, Chew, et al., PACE 1996; 19: 822–828), cardiac function was shown to have a diurnal or circadian variation. Moreover, when relying on any external hemodynamic monitoring system, the control parameters of the pacemaker or ICD cannot be automatically adjusted to respond to on-going changes in patient cardiac function. Accordingly, it would be desirable to provide a technique to assess cardiac function using the implanted cardiac stimulation device. In this manner, cardiac function can be automatically evaluated and mono or biventricular pacing control parameters adjusted in a closed loop system so as to permit optimal ventricular resynchronization therapy when the patient is upright as well as supine, at various times of the day and during various activities. It is to this end that further aspects of the invention are directed.
In particular, it would be desirable to provide a technique for assessing cardiac function using heart sounds detected internally by a pacemaker or ICD. Briefly, a first (S1) heart sound (HS) is associated with closure of the mitral valve but as the valve leaflets are tissue thin, other mechanical factors associated with the closure of the valve are believed to account for the audible sounds. These include the oscillation of blood in the ventricular chambers, vibration of the chamber walls, abrupt tensing of the chordae tendinae supporting the mitral valve leaflets and tensing of the mitral valve itself. A second (S2) heart sound is associated with closure of the aortic and pulmonic valves. Commonly, two distinct components of the second sound are audible with the aortic component preceding the pulmonic component in a normal heart. The cause of the sound is not the valve leaflets coming together. Rather, it is due to the sudden deceleration of backward blood flow after ventricular contraction has ended and stretching of the aortic and pulmonic walls by the attempted backward flow of blood. Normally, the aortic component precedes the pulmonic component. The two components may move further apart during inspiration and closer together during exhalation. When there is a delayed activation of the left ventricle as may occur with an intraventricular conduction abnormality such as left bundle branch block, the aortic component may follow the pulmonic component with S2 becoming single during inspiration and widely split during exhalation. Correlating with overall cardiac function are heart sounds in the absence of primary valve abnormalities. The intensity of S1 may vary with the AV delay as well as with the vigor of contraction. The timing of S2 may also vary with contractility and the relative coordination or lack of coordination of cardiac contraction.
To implement internal detection of heart sounds using a pacemaker or ICD, acceleration signals detected by an on-board accelerometer can be processed to derive heart sound signals. One exemplary technique for deriving heart sounds using an accelerometer of an implanted device is discussed in U.S. Pat. No. 5,935,081 to Kadhiresan. More specifically, in the technique of Kadhiresan, the accelerometer signal is filtered using a band-pass filter to derive heart sounds. However, high frequency heart noises due to rapid turbulent flow are not detected. Moreover, the heart sounds appears to be derived only for diagnostic purposes, i.e. heart sound data is merely transmitted to an external device for subsequent review. Although the filter-based technique of Kadhiresan may be effective for recording certain types of heart sound data for diagnostic purposes, it does not provide for the on-board evaluation of overall cardiac function or for the automatic adjustment of pacing control parameters to permit ventricular resynchronization therapy. Moreover, by filtering out noises associated with turbulent flow, the technique does not permit detection of heart murmurs and the like, which can be important in determination of appropriate therapy.
Another exemplary technique for deriving heart sounds using an accelerometer is discussed in U.S. Pat. No. 5,836,987 to Baumann et al. Although the technique of Baumann et al. provides for automatic adjustment of certain pacing parameters (such as AV intervals) based on heart sound signals, it does not appear to provide for ventricular resynchronization therapy. Also, although Baumann et al. discuss the adjustment of certain pacing parameters so as to optimize cardiac performance, the technique does not appear to provide any capability for actually evaluating overall cardiac output in terms of, e.g., stroke volume, cardiac output, or max dP/dt. Hence, overall cardiac function is not actually tracked and optimization of pacing parameters based on overall cardiac function is not achieved.
Accordingly, it would be desirable provide improved techniques for use with implantable devices that permit the detection of heart sounds and heart murmurs, that provide for evaluation of overall cardiac function particularly in terms of stroke volume, cardiac output, or max dP/dt, and that permit optimization of pacing control parameters to maximize overall cardiac output and not just individual heart sound parameters. Additional aspects of the invention are directed to those ends.